Exploring the mechanisms of magnolol in the treatment of periodontitis by integrating network pharmacology and molecular docking

Background: Magnolol, a bioactive extract of the Chinese herb Magnolia officinalis has a protective effect against periodontitis. This study is aimed to explore the mechanisms involved in the functioning of magnolol against periodontitis and provide a basis for further research. Methods: Network pharmacology analysis was performed based on the identification of related targets from public databases. The Protein-protein interaction (PPI) network was constructed to visualize the significance between the targets of magnolol and periodontitis. Subsequently, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed to predict the functions and the signal regulatory pathways involved in the action of magnolol against periodontitis. The "functiontarget-pathway" networks were constructed to analyze the core targets and pathways of magnolol against periodontitis. Molecular docking was used to verify the interaction of magnolol and core targets. Results: A total of 58 active targets of magnolol and 644 periodontitis-related targets were collected from public databases. A total of 25 targets of magnolol against periodontitis were identified based on the Venn diagram. GO analysis showed that magnolol has a role in the response to oxidative stress, nicotine, and lipopolysaccharide. KEGG enrichment analysis indicated that the mechanism of magnolol against periodontitis was mainly related to the tumor necrosis factor (TNF), phosphoinositide 3-kinase (PI3K/Akt), and mitogen-activated protein kinase (MAPK) signaling pathways. Combined with PPI network and molecular docking results, the core targets of magnolol against periodontitis included AKT1, MAPK8, MAPK14, TNF, and TP53. Conclusion: To summarize, the anti-periodontitis mechanisms of magnolol are potentially through regulating the TNF, PI3K/Akt, and MAPK signaling pathways.